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Dysbarism is commonly encountered in scuba divers and refers to complications associated with changes in environmental ambient pressure and with breathing compressed gases. These effects are governed by the gas laws: Boyle law states that pressure and volume are inversely related; Henry law states that, at equilibrium, the quantity of gas in solution is proportional to the partial pressure of that gas; Henry law states that total pressure exerted by a mixture of gases is the sum of the partial pressures of each gas.

Barotrauma is the most common diving-related affliction and is caused by the direct mechanical effects of pressure, as gas-filled cavities in the body contract or expand with pressure. The most common form of barotrauma occurs during descent and is middle ear squeeze, or barotitis media. It is caused by inability to equalize pressure causing tympanic membrane bleeding or rupture and may result in conductive hearing loss. A forceful Valsalva during equalization can cause inner ear barotrauma with rupture of the round or oval window. Symptoms include tinnitus, sensorineural hearing loss, and vertigo. If the sinus ostia are occluded on descent, an impending squeeze can cause bleeding from the maxillary or frontal sinuses, resulting in pain and epistaxis.

Barotrauma during ascent is due to expansion of gas in body cavities. In the middle ear, the pressure differential from asymmetrical expansion can cause alternobaric vertigo. Although rare, “reverse squeeze” may affect the ear or sinuses during ascent with rupture. Pulmonary overinflation or burst lung can occur during rapid, panicked ascents if divers fail to exhale or if intrinsic pulmonary air trapping exists (eg, COPD) resulting in pneumediastinum, subcutaneous emphysema or pneumothorax. The most serious consequence is cerebral arterial gas embolism (CAGE). Neurologic symptoms occur on ascent or immediately upon surfacing and include loss of consciousness, seizure, blindness, disorientation, hemiplegia, or other signs of stroke.

Divers using compressed air, caisson (tunnel) workers, and high-altitude pilots can all present with decompression sickness (DCS). In divers, this usually results from exceeding the dive table limits for depth and time. DCS can occur within minutes to hours of surfacing, rarely days later. Excessive bubble formation in tissue or circulation from saturated gas can cause both acute occlusive and delayed inflammatory effects. Type I DCS includes mottled skin and deep pain of the joints, usually the shoulder or knee, and is unaffected by movement. Type II, “serious,” DCS involves the central nervous system, typically the spine. Patients may initially complain of truncal constriction with ascending paralysis. Prolonged exposure at depth can lead to cardiopulmonary “chokes” or vestibular “staggers.” Because DCS and CAGE can be difficult to distinguish, or present simultaneously, the term “decompression illness” is now typically used.

Dive profile (depth, duration, and repetitiveness) and time of symptom onset are the most useful historical factors in distinguishing dysbarism from other disorders. During descent, the most common maladies are the squeezes. A fistula test, insufflation of the tympanic membrane ...